PRKCG Antibody

說明書

中文名稱：

PRKCG兔多克隆抗體
貨號：

CSB-PA210184
規(guī)格：

￥1100
圖片：
Gel: 10%SDS-PAGE, Lysate: 40 μg, Lane: Mouse brain tissue, Primary antibody: CSB-PA210184(PRKCG Antibody) at dilution 1/500, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 20 seconds
其他：

產品詳情
產品評價
相關產品
靶點詳情

產品詳情

Uniprot No.：

P05129
基因名：

PRKCG
別名：

KPCG_HUMAN antibody; MGC57564 antibody; OTTHUMP00000067291 antibody; PKC-gamma antibody; PKCC antibody; PKCG antibody; PRKCG antibody; Protein kinase C gamma antibody; Protein kinase C gamma polypeptide antibody; Protein kinase C gamma type antibody; Protein kinase C; gamma antibody; SCA 14 antibody; SCA14 antibody
宿主：

Rabbit
反應種屬：

Human,Mouse,Rat
免疫原：

Synthetic peptide of Human PRKCG
免疫原種屬：

Homo sapiens (Human)
標記方式：

Non-conjugated
抗體亞型：

IgG
純化方式：

Antigen affinity purification
濃度：

It differs from different batches. Please contact us to confirm it.
保存緩沖液：

-20°C, pH7.4 PBS, 0.05% NaN3, 40% Glycerol
產品提供形式：

Liquid
應用范圍：

ELISA,WB

推薦稀釋比：

Application	Recommended Dilution
ELISA	1:2000-1:5000
WB	1:500-1:2000

Protocols：

ELISA Protocol
Western Blotting (WB) Protocol
儲存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

功能：

Calcium-activated, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that plays diverse roles in neuronal cells and eye tissues, such as regulation of the neuronal receptors GRIA4/GLUR4 and GRIN1/NMDAR1, modulation of receptors and neuronal functions related to sensitivity to opiates, pain and alcohol, mediation of synaptic function and cell survival after ischemia, and inhibition of gap junction activity after oxidative stress. Binds and phosphorylates GRIA4/GLUR4 glutamate receptor and regulates its function by increasing plasma membrane-associated GRIA4 expression. In primary cerebellar neurons treated with the agonist 3,5-dihyidroxyphenylglycine, functions downstream of the metabotropic glutamate receptor GRM5/MGLUR5 and phosphorylates GRIN1/NMDAR1 receptor which plays a key role in synaptic plasticity, synaptogenesis, excitotoxicity, memory acquisition and learning. May be involved in the regulation of hippocampal long-term potentiation (LTP), but may be not necessary for the process of synaptic plasticity. May be involved in desensitization of mu-type opioid receptor-mediated G-protein activation in the spinal cord, and may be critical for the development and/or maintenance of morphine-induced reinforcing effects in the limbic forebrain. May modulate the functionality of mu-type-opioid receptors by participating in a signaling pathway which leads to the phosphorylation and degradation of opioid receptors. May also contributes to chronic morphine-induced changes in nociceptive processing. Plays a role in neuropathic pain mechanisms and contributes to the maintenance of the allodynia pain produced by peripheral inflammation. Plays an important role in initial sensitivity and tolerance to ethanol, by mediating the behavioral effects of ethanol as well as the effects of this drug on the GABA(A) receptors. During and after cerebral ischemia modulate neurotransmission and cell survival in synaptic membranes, and is involved in insulin-induced inhibition of necrosis, an important mechanism for minimizing ischemic injury. Required for the elimination of multiple climbing fibers during innervation of Purkinje cells in developing cerebellum. Is activated in lens epithelial cells upon hydrogen peroxide treatment, and phosphorylates connexin-43 (GJA1/CX43), resulting in disassembly of GJA1 gap junction plaques and inhibition of gap junction activity which could provide a protective effect against oxidative stress. Phosphorylates p53/TP53 and promotes p53/TP53-dependent apoptosis in response to DNA damage. Involved in the phase resetting of the cerebral cortex circadian clock during temporally restricted feeding. Stabilizes the core clock component ARNTL/BMAL1 by interfering with its ubiquitination, thus suppressing its degradation, resulting in phase resetting of the cerebral cortex clock.
基因功能參考文獻：
1. This review showed that the PKC Gamma signaling related genes and calcium signaling related genes then discuss their role for both Purkinje cell dendritic development and cerebellar ataxia. PMID: 28554312
2. SUMOylation of EphB1 repressed activation of its downstream signaling molecule PKC-gamma, and consequently inhibited neuroblastoma tumorigenesis. PMID: 29550816
3. two out of three known mutations in the catalytic domain of PKCgamma did indeed show increased biological activity. PMID: 28738819
4. The gene-environment combination of PRKCG rs3745406 C allele, BDNF rs6265 G allele and high level of negative life events was significantly associated with major depressive disorder. PMID: 26921055
5. The results showed that carrier of rs454006*C allele and rs3745406*C might elevate the risk of osteosarcoma PMID: 25663494
6. Data suggest that PRKCG (protein kinase C gamma) phosphorylates TA isoforms of p63 (tumor protein p63) at Thr157 to stabilize them and promote cell apoptosis in tumor cells. PMID: 26112605
7. PKCgamma,mutated in the neurodegenerative disease spinocerebellar ataxia type 14 is a novel amyloidogenic protein. PMID: 25217572
8. The rs454006 polymorphism of the PRKCG gene correlated to osteosarcoma susceptibility and might increase the risk of osteosarcoma. PMID: 25252845
9. findings provide evidence for both an increased PKCgamma activity in Purkinje cells in vivo and for pathological changes typical for cerebellar disease thus linking increased and dysregulated activity of PKCgamma to development of cerebellar disease PMID: 24937631
10. we show that the mutation V138E of the protein kinase C gamma (PKCgamma) C1B domain, which is implicated in spinocerebellar ataxia type 14, exhibits a partially unfolded C-terminus PMID: 24134140
11. PKCgamma plays a critical role in cancer cells, and simultaneous inhibition of PKCgamma and Hsp90alpha synergistically prevents cell migration and promotes apoptosis in cancer cells. PMID: 24117238
12. A novel missense mutation, F643L, which maps to a highly conserved amino acid of the catalytic domain of protein kinase C gamma, extends the phenotype associated with the spinocerebellar ataxia type 14 (SCA14) locus. PMID: 15313841
13. Spinocerebellar ataxia type 14 mutant PKC-gamma upregulates Hsp70. Hsp70 has a role in degrading mutant PKC-gamma. PMID: 24021284
14. Exome sequencing of large, 5-generational British kindred finds a novel p.Arg26Gly mutation in the PRKCG gene causing familial spinocerebellar ataxia 14. PMID: 22675081
15. SCA14, a novel mutation in the PRKCG gene, was found in two families in Norway with autosomal dominant cerebellar ataxia. PMID: 21434874
16. We propose that variety of mutant gammaPKC characters integrally and complicatedly participate in the pathophysiology of SCA 14. PMID: 21906004
17. The Spinocerebellar ataxia type 14 is caused by mutations in the protein kinase C gamma (PKCgamma, PRKCG) gene with a hotspot for mutations in exon 4. Genetic testing for SCA14 is clinically available. PMID: 21827914
18. Data show that through HINT1, the MOR facilitates the cross-talk of two NO- and zinc-regulated signal-transduction pathways, PKC/Src and Raf-1/ERK1/2, implicated in the negative control of morphine effects. PMID: 21235400
19. cPLA(2)-dependent AA release is required for VEGF-induced Src-PLD1-PKCgamma-mediated pathological retinal angiogenesis PMID: 21536681
20. These results indicate that autophagy contributes to the degradation of mutant gammaPKC, suggesting that autophagic inducers could provide therapeutic potential for SCA14. PMID: 20398063
21. Protein Kinase C gamma rs3745406 polymorphism is not significantly associated with major depressive disorder. PMID: 20627017
22. The presence of unphosphorylated PKC-gamma in HT29 cells, and its complete absence in Caco2 cells demonstrates a cell type-dependent differential coupling of Thr514-phosphorylation with de novo synthesis of PKC-gamma in colon cancer cells. PMID: 20188713
23. Missense mutations occur in the regulatory domain of PKC gamma: a new mechanism for dominant nonepisodic cerebellar ataxia. PMID: 12644968
24. Spinocerebellar ataxia(SCA) type 14 is caused by mutations in PRKCG gene. The observation that all 4 PRKCG mutations identified in patients with SCA to date are located in exon 4 suggests a critical role for this region of the gene in cerebellar function. PMID: 14676051
25. We sequenced exons 4 and 5 of PRKCG and detected a missense mutation in exon 4, involving a G-->A transition in nucleotide 353 and resulting in a glycine-to-aspartic acid substitution at residue 118 in a Dutch autosomal dominant cerebellar ataxia family PMID: 14694043
26. osmotic shock in human keratinocytes leads to activation of phospholipase C-gamma1 PMID: 15014953
27. spinocerebellar ataxia type 14 mutations make gammaPKC form cytoplasmic aggregates, which may play a role in development of SCA14 PMID: 15964845
28. Six mutations were found that segregated with the disease including F643L (exon 18), Five new missense mutations were identified in exons 4 (C114Y/G123R/G123E), 10 (G360S) and 18 (V692G). PMID: 16193476
29. These results indicate that PKCgamma regulates NMHC-IIB phosphorylation and cellular localization in response to EGF stimulation. PMID: 16394101
30. These results suggest that the PKC gamma R659S mutation is susceptible to neuronal death and is involved in the pathogenesis of neurodegenerative diseases, including Retinitis pigmentosa. PMID: 16828200
31. The present findings show that the interaction between PKCgamma and GluR4 is specifically required to assure PKC-driven phosphorylation and surface membrane expression of GluR4. PMID: 17233759
32. PRKCG mutation (SCA-14) causing a Ramsay Hunt phenotype. PMID: 17343273
33. detection of a new mutation in PRKCG responsible for spinocerebellar ataxia type 14, which may be located in a mutational hot spot PMID: 17562946
34. Codon 101 of PRKCG, a preferential mutation site in SCA14. PMID: 17659643
35. This study present a benign SCA14 phenotype in a German patient associated with a missense mutation in exon 3 of the PRKCG gene PMID: 17708558
36. PKCgamma, but not C1 domain mutants, inhibits Ca2+ influx in response to muscarinic receptor stimulation. PMID: 18499672
37. These studies suggest that Purkinje cell damage in SCA14 may result from a reduction of PKCgamma activity due its aberrant sequestration in the early endosome compartment. PMID: 18503760
38. The impact of three C1B regulatory subdomain mutations on the intracellular kinetics, protein conformation and kinase activity of PKCgamma in living cells, was investigated. PMID: 18577575
39. Rac regulates the interaction of fascin with active PKC. PMID: 18716283
40. study investigated whether mutant gammaPKC formed aggregates and how mutant gammaPKC affects the morphology and survival of cerebellar Purkinje cells (PCs), which are degenerated in SCA14 patients PMID: 19041943
41. Protein kinase C gamma, a causative for spinocerebellar ataxia, negatively regulates nuclear import of aprataxin. PMID: 19561170
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相關疾病：

Spinocerebellar ataxia 14 (SCA14)
亞細胞定位：

Cytoplasm. Cytoplasm, perinuclear region. Cell membrane; Peripheral membrane protein. Cell junction, synapse, synaptosome. Cell projection, dendrite.
蛋白家族：

Protein kinase superfamily, AGC Ser/Thr protein kinase family, PKC subfamily
組織特異性：

Expressed in Purkinje cells of the cerebellar cortex.
數據庫鏈接：

HGNC: 9402

OMIM: 176980

KEGG: hsa:5582

STRING: 9606.ENSP00000263431

UniGene: Hs.631564

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